Huang Zhihong, Chen Qing, Ma Liuhong, Chen Zhiming, Chen Wenpu, Qin Li, Jiang Jianwei
Department of Pulmonary Medicine, Jinan University, Guangzhou, China.
Nan Fang Yi Ke Da Xue Xue Bao. 2012 May;32(5):606-9.
To observe the effect of sodium valproate (VPA) on the proliferation and apoptosis of human lung carcinoma SPC-A1 cells and the underlying mechanism.
The effect of VPA on the proliferation of SPC-A1 cells was evaluated by MTT assay and clone formation assay. Flow cytometry was used to analyze the apoptosis of the cells exposed to VPA. The changes in the expressions of Bcl-xl, Bcl-2, Mcl-1, caspase-9, and caspase-3 in the exposed cells were detected by Western blotting.
Incubation with VPA for 48 h resulted in a significant inhibition of SPC-A1 cell proliferation, with a IC(50) of 1.8 mmol/L. VPA treatment also inhibited cell colony formation and induced obvious cell apoptosis. Exposure to 8 mmol/L VPA for 48 h caused a percentage of early apoptotic cells of 60.44%. VPA treatment at different concentrations for 48 h obviously lowered the protein levels of Bcl-xl, Bcl-2, and Mcl-1 and induced caspase-9 and caspase-3 activation in SPC-A1 cells.
VPA can inhibit the proliferation of SPC-A1 cells by triggering mitochondrion-dependent apoptosis.
